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Year 4 Small Animal Studies > Internal Medicine: Endocrinology: Adrenal Endocrinopathies > Flashcards

Internal Medicine: Endocrinology: Adrenal Endocrinopathies Flashcards

(41 cards)

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1
Q

What are the layers of the adrenal gland?

A
  • Capsule
  • Glomerulosa- cortex
  • Fasiculata- cortex
  • Reticularis- cortex
  • Medulla
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2
Q

What do the following layers of the adrenal gland show?
1. Glomerulosa
2. Fasiculata
3. Reticularis
4. Medulla

A
  1. Mineralocorticoids
  2. Glucocorticoids
  3. Androgens
  4. Adrenaline, nor-adrenaline
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3
Q

What are examples of mineralocorticoids

A

Aldosterone
* influence salt and water balance

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4
Q

What is an example of glucocorticoids?

A
  • Cortisol
  • Corticosterone
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5
Q

What are examples of androgens?

A
  • Testosterone
  • DHT
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6
Q

What is ACTH?

A

Adrenocorticotropic hormone

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7
Q

What is hyperadrenocorticism?

A

Over production of cortical (cortex) hormones

Cortisols the baddie

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8
Q

What are the different ways hyperadrenocorticism can be caused?

A
  • PDH- pituitary dependent HAC
  • ADH- adrenal dependent HAC
  • FAT- functioning adrenal tumour
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9
Q

What hormone is required for the production of cortisol and aldosterone?

A

Pregenalone

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10
Q

What are the effects of cortisol?

A
  • Breakdown of adipose to fatty acids
  • Affects hair follicles
  • Gluconeogenesis, insulin resistance
  • Reduced bone formation
  • Reduced calcium absorption in intestine
  • Down regulated the synthesis of collagen
  • Raises free amino acids in serum
  • Inhibits collagen formation
  • Decreasing amino acid uptake by muscle
  • Inhibits protein synthesis
  • Reduction of IgA, IgM IgE
  • Delayed wound healing
  • Increases water diuresis, GFR, renal plasma flow
  • Increases renal sodium retention of potassium excretion
  • Increases intestinal sodium and water absorption and potassium excretion
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11
Q

Who gets hyperadrenocorticism?

A
  • Medium to older age dogs
  • PDH: more common in small breeds
  • ADH: more common in large breeds
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12
Q

What are common clinical signs of cushings?

A
  • Polydipsia
  • Polyuria
  • Polyphagia
  • Panting
  • Abdominal distention
  • Endocrine alopecia
  • Hepatomegaly
  • Muscle weakness
  • Systemic hypertension
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13
Q

What would haematology, biochemistry and urinalysis show for cushings?

A

Haematology
* Neutrophilic leukocytosis
* Lymphopenia
* Eosinopenia
* Thrombocytosis
* Mild erythrocytosis

Serum biochemistry
* Increased ALKP
* Increased ALT
* Hypercholesteraemia
* Hypertriglceridaemia
* Hyperglycaemia

Urinalysis
* Specific gravity
* < 1.013- 1.02
* Proteinuria
* Urinary tract infection

Also- reduced T4, Normal TSH

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14
Q

How can cushings be definitively diagnosed?

A

Low dose dexamethasone supression test

  • 0.01mg/kg dexamethaons
  • Blood sample at 3 and 8 hours
  • Avoid feeding during test
  • High sensitivity
  • Lower but ok specificity

Best screening test

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15
Q

How is the ACTH stimulation test done?

A
  • 5 ug/kg ACTH
  • Blood sample at 0 and 1
  • Avoid feeding
  • Sensitivity higher for PDH
  • Specificity ok

Less effective

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16
Q

How can urine cortisol creatinine ratio be used for diagnosis of cushings?

A

Random sample- less sensitive/specific

Sampling 2 days after a clinical visit
Increases sensitivity/specificity

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17
Q

How can ACTH assay differentiate between PDH and FAT?

Study These Flashcards
A

normal 20-100 pg/ml
* PDH >45 pg/ml in 90%
* FAT < 20pg/ml in 70%

Imaging

18
Q

What is used to treat cushings?
What is the MOA?

Study These Flashcards
A

Trilostane

Competitively inhibits enzyme in adrenal cortex slowing production of cortisol production

19
Q

How is cushings treatment monitored?

Study These Flashcards
A
  • Clinical signs
  • ACTH stimulation test- 3 months for first year then 6
20
Q

What are other effects of trilostane?

Study These Flashcards
A
  • Adrenal necrosis
  • Hypoadrenocorticism
  • Lack of efficacy
  • Vomiting and Diarrhoea
21
Q

What is mitotaine used for in HAC?

Study These Flashcards
A

Cancer of the adrenal gland

(FAC)

22
Q

What frequently occurs with treatment of HAC and how it is treated?

Study These Flashcards
A

Hypertension

Benazepril

23
Q

When can surgery for HAC be used?

Study These Flashcards
A

Adrenal tumuors- if not invading renal vein or vena cava

Pituitary tumours- survival improving

24
Q
  1. What is macroadenoma?
  2. How is it diagnosed?
  3. How is it treated?
Study These Flashcards
A
  1. A benign tissue of the pituitary gland
  2. Patient gets duller when treated but ACTH stimulation and metabolic screens are good
  3. Hypophysectomy, radiotherapy
25
What disease can scottish terriers have that presents as HAC?
Hepatopathy Abnormal dynamic cortisol Don't need trilostane
26
What is addison's disease?
Hypoadrenocorticism
27
What is the aetiology of hypoadrenocortism?
Primary * Destruction of >90% of adrenal cortices * Multiple autoimmune-associated genes may be involved Secondary: * Defecit ACTH leading to atrophy of adrenal cortex * Primarily cortisol defiency
28
What is the most common signalment of hypoadrenocorticism?
* Uncommon * Middle aged female Breeds * Standard poodle * Beardies * Gt Dane * Portugese water dog * WHWT * St B * Wheaten * Rottie
29
What are the clinical signs of addisons?
Acute or chronic * Vague malaise * Vomiting and diarrhoea/Melaena * Lethargy/weakness * PUPD * Abdominal pain * Hypovolaemic collapse
30
What may be identified on physical examination of addisons?
* Weak pulses * Increased CRT * Dehydration * Bradycardia * Abdominal pain * Collapse/syncope
31
What can show on haematology and biochemistry for addisons?
* Mild non-regenerative anaemia * Mild hypercalcaemia * Pre-renal azotaemia * Lymphocytosis ± eosinophilia * Na:K ratio < 27:1 * Hyperkalaemia * Hyponatraemia * Isothenuric to hypesthenuric urine * Acidosis
32
What is atypical addisons?
* Cortisol defiency * Normal mineralocorticoids * Usually progress to mineralocorticoid deficiency
33
What are differentials for hyperkalaemia, hyponatraemia?
* GI disease * Renal failure * Parasitic infection- whipworms * Urinary obstruction * Chronic effusion with repeated drainage * Pregnancy * CHF * Diabetes mellitus * Chronic blood loss
34
How can hyperkalaemia present on ECG?
With increased hyperkalaemia * Bradycardia * Tall narrow T waves * Prolonged QRS interval * Decreased P wave * Prolonged P-R interval * Absent P wave * Complete heart block ventricular arrythmias
35
How can addisons be diagnosed and ruled out?
Endocrine testing * Single cortisol- addisons ruled out * < 55nmol will detect 100% addisons * High false positive
36
How does primary and atypical addisons differ? * Electrolytes * Pre/Post ACTH cortisol * Endogenous ACTH * Cortisol: ACTH * Aldosterone: Renin
Both * Pre ACTH cortisol- low * Post ACTH low * Endogenous ACTH- high * Cortisol: ACTH- low * Aldosterone: Renin- low Primary- electrolytes abnormal Atypical- electrolytes normal
37
How does secondary addisons differ to primary: * Electrolytes * Pre/Post-ACTH cortisol * Endogenous ACTH * Cortisol:ACTH * Aldosterone:Renin
Electrolytes * P- abnormal * S- normal Pre/Post ACTH cortisol * Both low Endogenous ACTH * P- high * S- low Cortisol:ACTH * P- low * S- high Aldosterone:Renin * P- Low * S- high
38
How is addisons disease treated?
Fluid therapy- * shock rates initially Hyperkalaemia- * dextrose saline + insulin, * calcium gluconate Steroid * Dexamethasone sodium phosphate * Hydrocortisone * Prednisolone sodium succinate * Once eating- oral pred, fludrocorstisone Maintenance therapy * Oral pred- maybe only when stressed * Fludrocortisone * DOCP- desoxycorticosterone privilate Life long therapy
39
What are potential problems with addisons treatment?
* Acute renal failure * Myelinosis Prevention- raise sodium slowly
40
1. What is phaeochromocytoma? 2. What are the clinical signs? 3. How is it diagnosed? 4. How is it treated?
1. Tumour of adrenal medulla secreting catecholamines 2. Episodic: Anxiety, tachycardia, tachypnoea, vomiting, diarrhoea, weight loss, hypertension 3. Radiography/US 4. Radical excision, antihypertensive
41
1. What causes hyperaldosteronism? 2. What are the clinical signs? 3. How is it treated?
1. Adrenal tumour- produces aldosterone 2. PUPD, weakness, hypokalaemia, hypotension 3. Restrict sodium, supplement potassium, surgical excisoin, spironolactone

Year 4 Small Animal Studies (97 decks)

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